The modulation of neutrophil (PMN) function has been studied by assessing chemoattractant receptors, cytoskeleton function, chemotaxis, degranulation and oxidative metabolism in normal and abnormal cells. The data indicate there is an intracellular pool of receptors for the chemoattractant fmet-leu-phe with the density of specific granules that are mobilized to the plasma membrane with cell activation. These data, together with studies in a patient with specific granule deficiency, support the concept that specific granules are a reservoir of receptors. In studies of factors regulating chemotaxis abnormal "turn-off" of acute inflammatory reactions was seen in chronic granulomatous disease and a select defect in PMN superoxide generation was seen in pregnancy. Incubation of monocytes from patients with Job's syndrome with Staphylococcus aureus was shown to release an inhibitor of PMN chemotaxis. In other studies levamisole was found inferior to placebo in preventing infections in patients with Job's syndrome. New approaches for pharmacologic manipulation of phagocyte function were explored using Vitamin K. Vitamin K inhibited chemotaxis and oxidative metabolism without altering chemoattractant, Fc, or C3b receptor expression. The possibility Vit K or closely related compounds may be useful is currently under investigation.